S Foote.
Experienced Member
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- 66
Of course there are genetic differences in cellular aging. Like I said before, cellular aging is heavily influenced by the environment. Did you know metabolism is one of the main causes of cellular aging? You can adjust your metabolism via calorie intake. Caloric deficits are proven to extend life. At the same time, chronic caloric surplus decreases lifespan by increasing cell division and also increasing metabolism byproducts. Reactive oxygen species are a byproduct of metabolism, which can lead to increased oxidative stress. Intake of antioxidants via diet can help alleviate this. Of course, the natural base antioxidant capacity differs from people to people, but it is also heavily influenced by diet.
Inflammation and toxins will also result in premature cellular aging. Again, this is environmental. Of course nothing will stop the natural aging process, but to say environmental factors have an insignificant impact is erroneous.
There is increasing evidence that gut flora imbalance and western diets play a large role in the increase in autoimmune diseases and allergies. Again, this is environmental. Your gut health is heavily related to mental health and also the immune system. Gut flora is all environmental, and not genetic.
In addition, the evidence for the correlation between metabolic syndrome, CVD, and Androgenetic Alopecia is undeniable now. It is not some small studies drawing vague correlations. You can look up the large amount of studies from accredited journals yourself.
If there is a problem to be solved, then you ask questions; you don't keep denying things or you will get nowhere. The DHT theory is in no way complete; that is why you have keep investigating. Going back to the CVD relation, your can either say "correlation not causation" and abandon the research right there and just wait for an answer, or you can continue investigating.
What if I told you there are studies showing those with Androgenetic Alopecia are more likely to have hypertension? Just a correlation? What if I tell you that studies show those with hypertension have higher serum IL-6 and inflammation, and that IL-6 is the main inflammatory cytokine involved in the hair loss cascade? What if I also tell you that in vitro studies show that IL-6 upregulates androgen receptors? Still just an insignificant correlation?
How about in vitro study demonstrating a greater sensitivity to oxidative stress in balding scalp derma papilla cells vs nonbalding cells? No significance? How about an in vitro study demonstrating that oxidative stress can upregulate TGF-beta, the cytokine responsible for fibrosis? TGF-beta is also part of the androgen cascade, and suppresses hair growth.
If you look into the biochemical implications of this blood flow study, then you will see why this is significant. Optionally, you can continue to dismiss it.
The point is, hair follicle miniaturisation by the normal spatial growth controls, explains all this. It gives order and logic to these subsequent events, and indicates what is or is not relevant.